GLYCOSYLATED HEMOGLOBIN LEVEL AND CAROTID INTIMAL-MEDIAL THICKENING IN NONDIABETIC INDIVIDUALS - THE ATHEROSCLEROSIS RISK IN COMMUNITIES STUDY

OBJECTIVE - People with diabetes are at increased risk for cardiovascu lar events. However, questions remain about what role, if any, homeost atic glucose control plays in the development of cardiovascular diseas e among nondiabetic individuals. we investigated the relationship betw een HbA(1c) level and carotid intimal-medial thickening in normoglycem ic individuals. RESEARCH DESIGN AND METHODS - We conducted a case-cont rol study among 208 normoglycemic individuals (fasting glucose less th an or equal to 6.4 mmol/l and no history of diabetes) who had carotid intimal-medial thickening (case subjects) and 208 normoglycemic contro l subjects individually matched for age, sex, race, field center, and date of exam. Subjects were free-living men and women, aged 45-64 year s at baseline, who participated in the Atherosclerosis Risk in Communi ties (ARIC) Study. RESULTS - HbA(1c), levels, expressed as percent of total hemoglobin, ranged from 4 to 7% and correlated only modestly wit h single measurements of fasting glucose (r = 0.16) and fasting insuli n (r = 0.14). The mean level of HbA(1c) was 5.18% among case subjects and 5.07% among control subjects (P = 0.004, paired t test). As compar ed with the first quartile of HbA(1c), the matched relative odds of be ing a case were 1.15, 1.33, and 2.30 for the second, third, and fourth quartiles, respectively (P = 0.005 for linear trend). After multivari ate adjustment for age, fasting glucose, fasting insulin, BMI, smoking status, hypertension, LDL cholesterol, HDL cholesterol, fibrinogen, a nd education level, the respective relative odds estimates were 0.98, 1.07, and 1.88 (P = 0.16 for linear trend). When modeled linearly as a continuous variable and after adjustment for the above-mentioned cova riates, a 1% point increment in HbA(1c) level was associated with 1.77 greater odds of being a case (95% CI, 0.9-3.5). CONCLUSIONS - These d ata provide some support to the hypothesis that in the absence of diab etes, homeostatic glycemic control is a risk factor for atherosclerosi s.